Obstruction of the Ureter - Causes, Signs and Symptoms.

Introduction:

Ureteral obstruction represents one of the most prevalent issues that urologists face. It can be caused by a multitude of factors, including both intrinsic and extrinsic renal disorders. The postobstructive pathophysiology varies based on whether one or both ureters were blocked. Preliminary data shows that atrial natriuretic peptide may have a role in postobstructive diuresis and protection against nephron ischemia in acute blockage. The possibility of renal function recovery following the obstruction removal is determined by the duration and severity of the blockage, the status of the contralateral kidney (another kidney), and the presence or absence of infection. The ability to acidify urine to pH 6.0 before surgery may indicate an obstructed kidney's recovery potential. Urologists may treat ureteral blockage with minimum intervention and preserve renal function using ureteral stents.

What Are the Possible Causes of Obstructive Nephropathy?

Kidney:

• Congenital Causes - Polycystic disease of the kidney, renal (kidney) cyst, fibrous blockage at the ureteropelvic junction, the peripelvic cyst, and the formation of abnormal vessels at the ureteropelvic junction.

• Neoplastic Causes - Wilms tumor, renal cell carcinoma, transitional-cell carcinoma involving the renal pelvis, and multiple myelomas.

• Inflammatory Cause - Tuberculosis or Echinococcus infection.

• Metabolic Cause - Formation of the calculi.

• Miscellaneous Causes - Aneurysm of the renal artery, trauma, and sloughed papillae.

Ureter:

• Congenital Causes - Stricture, ureterocele, reflux of the ureter, ureteral valve abnormalities, ectopic kidney, retrocaval ureter, and Prune belly syndrome.

• Neoplastic Cause - Primary or metastatic ureteral carcinoma

• Inflammatory Causes - Tuberculosis or schistosomiasis infection, abscess, cystic ureteritis, and endometriosis (is characterized by the presence of the uterus lining outside the uterus).

• Miscellaneous Causes - Fibrosis of the retroperitoneum, aneurysm of the aorta, radiation treatment, lymphocele, trauma, urinoma, and pregnancy.

Bladder and Urethra

• Congenital Causes - Posterior urethral valve, phimosis (A condition in which skin over the head of the penis is tight and cannot be pulled back), urethral stricture (scarring and narrowing of the tube (urethra) that carries urine out of your body), hypospadias (A condition in which the opening urethra is not positioned at the tip of the penis), epispadias (the urethra does not develop fully into a tube, and urine is passed out of the body from an abnormal location), hydrocolpos (defects formed by congenital malformations that induce vaginal and uterine retention and buildup of cervicovaginal secretions).

• Neoplastic Causes - Carcinoma of the urethra, bladder, prostate, and penis.

• Inflammatory Causes - Prostatitis (inflammation of the prostate gland), and abscess of the paraurethral.

• Miscellaneous Causes - Prostatic hyperplasia of benign origin, and neurogenic bladder.

What Are the Signs and Symptoms of Obstructive Uropathy?

Signs of Obstructive Uropathy:

• Abdominal or flank mass is palpable.

• Metabolic acidosis with hyperkalemia and hyperchloremic (an abnormality in potassium and chloride ions).

• Wastage of salt.

• Hematuria (blood in the urine).

• Hypertension.

• Proteinuria (excessive proteins in the urine).

Symptoms of Obstructive Uropathy:

• Pain in the abdomen.

• Changes in Urinary output.

• Urinary tract infections that reoccur.

• Enuresis (loss of bladder control during the night).

• Nocturia (increased frequency of urine at night).

• Dysuria (Pain during urination).

• Increased frequency of urination.

What Is Acute Unilateral Ureteral Obstruction?

• There is an immediate and dramatic increase in ureteral pressures following acute unilateral blockage; the actual rise depends on the patient's hydration condition at the time of the obstruction.

• Minutes after the acute blockage, ureteral pressures may rise to 50 to 70 mm Hg (normal 6.5 mm Hg). This high pressure is passed back into the kidney, causing an immediate decrease in the glomerular filtration rate (GFR).

What Are the Physiological Changes of Acute Unilateral Ureteral Obstruction?

• During the early stages of ureteral blockage, prostaglandin E2 (PGE2) levels rise. It serves as a vasodilator in the afferent arterioles, enhancing renal blood flow and it might be a homeostatic effort to preserve a normal GFR.

• The increased blood flow raises the intrapelvic and intraurethral pressures even more. Higher pressures strain mechanoreceptors on the ureteral wall and renal capsule, resulting in the extreme pain of ureteral colic.

• Treatment with Indomethacin, a powerful cyclooxygenase inhibitor that reduces prostaglandin production, can prevent the rise in blood flow.

• Inhibiting prostaglandin production can treat the underlying pathophysiologic mechanism of renal colic rather than just reducing its discomfort with opioid analgesia.

• Nonsteroidal anti-inflammatory drugs (NSAIDs) are well-known inhibitors of prostaglandin production. Prostaglandin synthetase inhibitors, such as NSAIDs, are safe as prostaglandin synthetase inhibitors in Scandinavia.

• Both oral and suppository Indomethacin has been shown to reduce the requirement for narcotic analgesia during acute ureteral colic and may cure colic resistance to drugs.

What Is the Mode of Blood Flow in the Acute Unilateral Ureteral Obstruction?

• In acute ureteral blockage, a triphasic pattern of renal blood flow appears. Flow increases within the first several hours. Flow declines slowly throughout the second phase (two to six hours).

• However, ureteral pressures continue to rise throughout this time, indicating that efferent arteriole vasoconstriction is trying to preserve a normal GFR (glomerular filtration rate) where afferent vasodilation has failed.

• The third or chronic phase occurs after about six hours, with a continuing decline in renal blood flow. However, at this period, ureteral pressures peak and begin to fall. These alterations have been linked to increased afferent arteriolar resistance.

What Is Chronic Unilateral Obstruction?

• Chronic unilateral ureteral obstruction, as seen in prostate cancer and staghorn calculi, prolongs the acute phase of unilateral blockage.

• Despite the persistent blockage, ureteral pressures continue to fall, and after eight weeks, the pressure is about 15 mm Hg.

• This pressure reduction is therapeutically relevant since individuals with persistent blockage may experience little or no pain following the initial colic episode. The blockage may then become clinically quiet, culminating in nephron destruction.

What Is the Mode of Blood Flow in Chronic Unilateral Obstruction?

• During chronic blockage, renal blood flow gradually declines. Renal blood flow is 50 percent of normal after 24 hours, 30 percent after six days, 20 percent at two weeks, and 12 percent at eight weeks.

What Are the Long-Term Effects of Chronic Unilateral Obstruction?

• The urologist is well aware of the long-term pathologic implications of renal obstruction: the pelvis and calyces enlarge, the medulla may be damaged, and the cortex may be restricted to a narrow margin of functional parenchyma. The ureter proximal to the blockage dilates during this early phase.

• One exception to this dilation arises when the ureter is mechanically unable to dilate due to external compression, as observed in retroperitoneal fibrosis or an encasing tumor mass.

• A urine leak caused by a rupture of fornical may also develop in a system with an acute high-grade blockage, and considerable dilatation may not be noticed. Ureteral dilatation stabilizes after ureteral pressures reach their apex.

• Even when the bladder is completely blocked, modest volumes of pee are generated. The majority of fluid reabsorption happens through venous backflow.

What Are Bilateral Ureteral Obstruction?

• Bilateral ureteral blockage generally appears gradually. The ureters might be physically blocked by locally invasive or metastatic cancer, or they can be functionally obstructed by benign prostatic hyperplasia silently or a decompensating neurogenic bladder.

• Before the emergence of acute renal failure caused by total bilateral blockage, clinical indicators of partial bilateral obstruction may be absent.

• Initial pathologic alterations were found in chronic bilateral blockage in newborns and adults. The chronic polyuria caused by this impairment might be the presenting sign. The diuresis that occurs with partial bilateral blockage is a water diuresis, as opposed to postobstructive diuresis, which includes a significant natriuresis.

• Patients who are not able to receive water, such as babies, elderly patients with decreased mental capacity, or postoperative or hospitalized patients, may suffer from severe dehydration. This polyuria is similar to nephrogenic diabetes insipidus in that it is resistant to vasopressin (ADH) injection through the distal tubule.

• Urine acidification impairment is a prevalent complaint in individuals suffering from bilateral ureteral obstruction.

What Are the Physiologic Changes of Bilateral Ureteral Obstruction?

• The physiologic consequences of bilateral and unilateral ureteral blockage vary markedly. Intratubular pressure rebounds to near-normal values in unilateral occlusion. Therefore, intratubular pressures remain larger than twice normal with bilateral occlusion within 24 hours.

• Although bilateral blockage reduces renal blood flow to a level equivalent to unilateral obstruction, the processes may be distinct. The single-nephron GFR was diminished in animals with unilateral blockage because of increased afferent arteriole resistance and a drop in glomerular plasma flow.

• In contrast, in animals with bilateral blockage, the reduction in single-nephron GFR was entirely due to higher intratubular pressures; afferent arteriole resistance and glomerular plasma flow were normal.

How Is the Recovery of Function after the Release of Ureteral Obstruction?

• The most appropriate medical concern for the urologist is the restoration of renal function following a period of blockage. Many factors influence recovery, including the duration and severity of the blockage, the presence of a normal contralateral kidney (in unilateral obstruction), and the presence or absence of infection.

• Chronic partial blockage, as observed in older men with prostatism and individuals with metastatic cervical, prostate, or colon cancer, can result in a decline in renal function, the amount of the damage is determined by the degree and duration of the obstruction. A study of older men with azotemia and prostatism discovered that the majority of the improvement in renal function happened within two weeks of establishing bladder drainage; minimal improvement occurred beyond two weeks.

Conclusion:

Recently, radionuclide scans were used to estimate function recovery following a blockage. Short-term nephrostomy tube drainage with creatinine clearance measurements has been identified as the greatest predictor of renal function recovery in the postobstructive kidney. Function recovery is a major problem for urologists. Excretory urograms and renal histology examinations have been ineffective